RESISTANCE OF DIFFERENT STOCKS AND TRANSFERRIN GENOTYPES OF

COHO SALMON, ONCORHYNCHUS KISUTCH, AND STEELHEAD TROUT,

SALMO GAIRDNERI, TO BACTERIAL KIDNEY DISEASE AND VIBRIOSIS 1
GARY W. WINTER, CARL B. ScHRECK, AND JOHN

D. McINTYRE 3

ABSTRACT
Juvenile coho salmon and steelhead trout ofdifferent stocks and three transferrin genotypes (AA, AC,
and CCl, all reared in identical or similar environments, were experimentally infected with
Corynebacterium sp., the causative agent of bacterial kidney disease, or with Vibrio anguillarum, the
causative agent of vibriosis. Mortality due to the pathogens was compared among stocks within a
species and among transferrin genotypes within a stock to determine whether there was a genetic basis
for resistance to disease. Differences in resistance to bacterial kidney disease among coho salmon
stocks had a genetic basis. Stock susceptibility to vibriosis was strongly influenced by environmental
factors. Coho salmon or steelhead trout of one stock may be resistant to one disease but susceptible to
another. The importance of transferrin genotype of coho salmon in resistance to bacterial kidney
disease was stock specific; in stocks that showed differential resistance of genotypes, the AA was the
most susceptible. No differences in resistance to vibriosis were observed among transferrin genotypes.

Bacterial kidney disease (BKD) caused by

Corynebacterium sp. is a major cause of serious
losses among salmon reared in freshwater
hatcheries of the Pacific Northwest (Leitritz and
Lewis 1976), and epizootics caused by Vibrio
anguillarum in the marine environment are
particularly devastating to salmonids maintained
in saltwater impoundments (Fryer et al. 1972).
Externally applied antibiotics are relatively
ineffective in the treatment of these diseases.
Immunization with bacterins for the control of
vibriosis has been shown to be feasible (Fryer et al.
1976), but attempts to produce a bacterin for BKD
have been unsuccessful (Evelyn 1977). The use of
disease resistant populations of fish may conceivably reduce the incidence and severity of these
diseases. Fish that inherit natural resistance to a
disease normally maintain that resistance
throughout their lives (Snieszko et al. 1959). In
addition, information on the resistance of donor
stocks, for use in transplants to infected waters,
would be valuable.
10regon Agricultural Experimental Station Technical Paper
No. 4862.
-Oregon Cooperative Fishery Research Unit, Oregon State
University, Corvallis, OR 97331. Cooperators are Oregon State
University, Oregon Department of Fish and Wildlife, and U.S.
Fish and Wildlife Service.
aoregon Cooperative Fishery Research Unit; present address:
U.S. Fish and Wildlife Service, Box 1050, Tyler Road, Red Bluff,
CA 96080.
Manuscript accepted Ma)' 1979.
FISHERY BULLETIN: VOL. 77, NO.4, 1980.

The existence ofdisease resistant strains within

a species has been demonstrated. Stock or strain
refers to a population of fish of one species which
shares both a common environment (a particular
stream) and common gene pool (discrete breeding
group) and, as such, can be considered as a
self-perpetuating system (Larkin 1972).
Differences in susceptibility to ulcer disease and
furunculosis have been observed among different
strains ofbrook trout, Salvelinus fontinalis (Wales
and Berrian 1937; Wolf 1954; Snieszko 1957;
Snieszko et al. 1959), and Gjedrem and Aulstad
(1974) noted significant differences in resistance
to vibriosis, which they showed to be slightly
heritable, between different strains of Atlantic
salmon, SaZmo saZar, parr in Norway.
Unfortunately, in most previous studies ofdisease
resistance, fish of the different stocks were not
reared in a common environment. Since
phenotypic expression is a combination of
genotype, environment, and interactions between
these two variables, different stocks must be
reared under identical conditions if one is to be
certain that differences in resistance to disease are
genetic in origin and not due, for example, to
previous exposure of a particular stock to the
disease in question or some other factor such as
nutritional history. One objective of the present
study was to determine whether there are
differences in resistance to BKD and vibriosis
795

FISHERY BULLETIN: VOL. 77, NO.4

among stocks of coho salmon, Oncorhynchus

kisutch, and steelhead trout, Salmo gairdneri, and
whether these differences have a genetic basis.
Suzumoto et al. (1977) reported differences in
resista,nce to BKD among three genotypes of
transferrin (an iron-binding plasma protein) in
coho salmon. In mammals, iron is known to
increase the growth and virulence of some
pathogens. Transferrin may reduce infection by
binding the metal, thereby reducing its
availability to invading bacteria, a process known
as nutritional immunity (Weinberg 1974). No iron
requirement has been demonstrated for BKD
bacteria, although it is likely that one exists,
judging by the fastidiousness of the organisms.
Hershberger (1970) observed differences in iron
binding capacity among transferrin genotypes in
brook trout and suggested that individuals more
efficient in the uptake and release of iron might
fare better under "adverse conditions" such as
disease. A second objective of this study was to
compare resistance to BKD and vibriosis among
transferrin genotypes, to evaluate earlier results
with BKD, and to determine whether transferrin
increases the tolerance of bacterial diseases of
salmonids in general. We also sought to determine
whether differences in resistance of transferrin
genotypes exist among different stocks of coho
salmon and steelhead trout.

MATERIALS AND METHODS

Juvenile coho salmon were obtained as eyed
eggs from the Fall Creek (Alsea) and Big Creek
salmon hatcheries, Oreg. The Big Creek hatchery
was also the source oftwo crosses, Big Creek x Sol
Duc (B x S) and Big Creek x Umpqua (B x U). All
stocks were reared at Corvallis, Oreg.-the Big
Creek stock at Oregon State University's Smith
Farm; the Alsea stock at the Oregon Department
of Fish and Wildlife's Research Section; and the
two crosses at Oregon State University's Fish
Disease Laboratory. These rearing facilities
presented similar, though not identical,
environments for the fish. Because we lacked
sufficient fish ofthe two crosses to include them in
all studies, we used them only in the BKD study.
Steelhead trout were obtained as green eggs
from the following Oregon State hatcheries: Alsea
(winter run), Roaring River (Siletz summer run),
Cole Rivers (Rogue summer run), and Marion
Forks (North Santiam winter run). All four stocks
796

were reared under identical conditions at Smith

Farm.
For determination of the transferrin genotypes
ofthe experimental fish, we withdrew about 0.1 ml
of blood from the caudal vein of anesthetized fish
with a 1 ml tuberculin syringe and ejected it into
heparinized hematocrit tubes, which were then
centrifuged. The plasma from the salmon was
frozen until the time of analysis. Blood samples
from steelhead trout were placed on ice and
processed within 4 h after collection because we
found that frozen storage reduces the stability of
transferrin in this species. Fish were individually
identified by dangler tags applied immediately
behind the dorsal fin .. We used starch-gel
electrophoresis, adapting the discontinuous buffer
system described. by Ridgeway et al. (1970), to
determine transferrin genotypes. Only the AA,
AC, and CC genotypes were considered, and in
some stocks only two of these were used. The
transferrins of Siletz and North Santiam
steelhead trout stocks were not included in this
study because resolution on the electrophoretic
gels was poor. After the fish were bled, they were
given a recovery period of at least 2 wk before they
were transferred to experimental tanks.

Bacterial Kidney Disease

All experimental fish were held indoors in 70 I
fiber glass tanks supplied with flowing, aerated,
chilled (122 C), dechlorinated water. The fish
were allowed to acclimate in these tanks for 2 wk.
Fish were fed once daily with Oregon Moist Pellet.
Each stock of coho salmon and steelhead trout
consisted of 125 fish divided into two test
replicates of50 each plus 25 control fish. Included
in the steelhead trout experiment was one group of
34 fish of hatchery-reared (Cole Rivers) Rogue
River stock, without a replicate. The respective
transferrin genotypes were distributed randomly
among all tanks.
The BKD (Corynebacterium sp.) strain
(RB-1-73) used was isolated on cysteine serum
agar from a spring chinook salmon, O.
tshawytscha, at the Round Butte Oregon State
Hatchery by J. E. Sanders, fish pathologist,
Oregon Department of Fish and Wildlife. A stock
culture was maintained on Mueller-Hinton agar
(Difco Laboratories,4 Detroit, Mich.) enriched
'Reference to trade names does not imply endorsement by the
. National Marine Fisheries Service, NOAA.

WINTER ET AL.: RESISTANCE OF COHO SALMON AND STEELHEAD TROUT

with cysteine (0.1%) and calf serum (20%). Before

each experiment, cells were passed once in the
species being tested to produce a fresh isolate, and
this isolate was further cultured until sufficient
cells were available for an inoculum.
All test fish received an intraperitoneal
injection of 0.1 ml ofa suspension ofkidney disease
bacteria in phosphate-buffered saline (PBS), and
all control fish received a 0.1 ml intraperitoneal
injection of only PBS. The approximate inocula
were 9 x 107 cells for the coho salmon (mean
weight, 23 g), and 3 x 108 cells for the steelhead
trout (mean weight, 36 g). The coho salmon were
injected on 17 March 1977 and the steelhead trout
on 12 September 1977. We examined all fish that
died and identified BKD as the causative agent on
the basis of presumptive diagnosis, using gram
stains of kidney smears. In addition, kidney
smears from 10% of the fish that died were
cultured on Mueller-Hinton media. Experiments
were terminated at the ,end of 4 mo or earlier,
depending on the progress of infection.
One week after the coho salmon had been
injected, an accidental exposure of the fish,
including the controls, to chlorine resulted in
mortalities as high as 50% in some stocks. The
study was nevertheless continued, but a second,
abbreviated test was begun on 24 August 1977.
Only Alsea and Big Creek stocks (mean weight,
33.2 g) were used; the Big Creek fish were obtained
directly from the hatchery. The inoculum for this
second experiment was increased to 3 X 108 cells.

Vibriosis
The V. anguillarum strain (LS-174) used in
these experiments was isolated on brain heart
infusion agar from a coho salmon at Lint Slough,
Waldport, Oreg., by J. S. Rohovec. The inocula
were either prepared from lyophilized cells or
recent passage isolates. Experimental fish were
exposed to the pathogen in 93 I stainless steel
tanks at Oregon State University's Fish Disease
Laboratory.
Two experiments were undertaken with the
coho salmon. In the first (8 October 1976),225 fish
(mean weights for Big Creek and Alsea stocks
were 10.4 g and 14.5 g, respectively) from each
stock were divided equally among two test
replicates and an untreated control. The three
tanks contained fish from each stock to insure
identical treatment. The fish in this experiment,
having not been bled and tagged for transferrin

genotype identification, were freeze branded to

differentiate the stocks in each tank. In the second
experiment (10 June 1977) the number offish per
tank was reduced to about 25 (mean weight, 36.6
g) because larger numbers were not available, but
transferrin genotypes had been determined.
In the steelhead trout phase of the study (21
October 1977), 75 fish from each stock (mean
. weight, 36 g) were divided equally among three
test replicates and 15 from each stock were placed
in a fourth tank for controls. A hatchery-reared
Rogue stock was also used in this steelhead trout
experiment. In a second experiment (27 December
1977) in which we used steelhead trout from the
Cole Rivers (Rogue), Alsea, and Marion Forks
(North Santiam) hatcheries, 50 fish (mean weight,
42.2 g), were divided equally between two
replicates. Transferrin genotypes were
distributed randomly among the tanks.
The initial temperature in all experimental
tanks was 12.2 C, to which all fish had been
acclimated. The temperature was then raised to
17.7 C over a period of 1.5 h, and at this
temperature water flow was discontinued in all
tanks for 15 min. The bacteria suspended in brain
heart infusion broth (Difco Laboratories) were
then introduced into the test tanks (other than
those of the controls). The inocula were 5 x 106
cells/ml for the first coho salmon exposure and 8.6
x 106 cells/ml for the second; the steelhead trout
received concentrations of8.8 x 106 cells/ml in the
first experiment and 7.2 x 106 cells/ml in the
second. All fish that died were necropsied and
kidney smears were cultured on brain heart
infusion agar. Positive diagnosis of V.
anguillarum was confirmed by slide agglutination
with specific antiserum. The experiments were
terminated at the end of 1 wk.
Statistical comparison of three or more stocks
involved a one-way analysis of variance based on
arcsin transformations of percentages and least
significant difference, and comparisons of
transferrin genotypes of two stocks were based on
X2 test employing a 2 x k contingency table
(Snedecor and Cochran 1967).

RESULTS AND DISCUSSION

Bacterial Kidney Disease
In the first experiment in which coho salmon
were infected with BKD, the Alsea stock and B x
U cross were about twice as resistant to the disease
797

FISHERY BULLETIN: VOL. 77, NO.4

as were fish of the Big Creek stock and B x S cross

(see totals, Figure 1A). The difference in mortality
between the B x U and each of the two more
susceptible groups (Big Creek and B x S), was
significant (P<O.05), but the Alsea mortality was
significantly lower than that of only the B x S,
cross (P<O.06). A comparison of mean times to
death (days) revealed a similar pattern: B x S,
79.5; B xU, 99.9; Big Creek, 88.4; and Alsea, 95.4.
The mean times to death for the B x U and Alsea
coho salmon were significantly greater than the B
x S (P<O.05). The differential resistance of coho
salmon stocks to BKD probably has a genetic basis

because the stocks were reared in similar

environments.
Among transferrin genotypes, only the B x S
cross and Alsea stock showed any important
differences in resistance to BKD (Figure 1A). In
both groups the AA genotype was the most
susceptible, and the AC and CC both showed
lower, similar mortalities. The difference in
resistance was significant (P<O.07) between the
AA and AC genotypes within the B x S cross. The
Alsea transferrin results, though not significant
due to small sample size, are substantiated by a
previous study in which Suzumoto et al. (1977)

BKD-coho

100

23
42

<l:
w

<l:
w

30

58

22

28

50

12

30

a:

w
a.

48

STOCK

AA AC

BxS

BxU

AA AC

101

BIG CR.

c
100

a.

III III
T

....
zw
a:

33 35 72

GENOTYPE AA N: CC

65

12

50

19 44 63

'5

..,.

BKD-coho

100

II

AAACCC
ALSEA

GENOTYPE AA AC
STOCK

BIG CR.tH)

AC CC

ALSEA

BKD-steelhead
34

26

74
74 100
96

<l:
w

FIGURE I.-Percentages of fish of different stocks and transferrin genotypes

that died of bacterial kidney disease (BKD). A and B, coho salmon experi
ments I and 2; C, steelhead trout experiment. T indicates total mortality for
the stock which sometimes includes fish with unknown genotypes; AA, AC,
and CC indicate mortality for individual genotypes; B x S = Big Creek x Sol
Due cross and B x U = Big Creek x Umpqua croBB; (Ii) indicates hatcheryreared fish. Numbers above bars show sample sizes; the vertical line above
each bar represents the upper limit of the 95% confidence interval.

50
IZ
w
U

a:

UJ

a.

GENOTYPE
STOCK

798

ROGUE ROGUE1H)

AC CC
ALSEA

T
NSAN

T
SILETZ

WINTER ET AL.: RESISTANCE OF COHO SALMON AND STEELHEAD TROUT

used Alsea coho salmon in which the AA genotype

was also the most susceptible to BKD. Because of
similar transferrin results in the B x S cross and
Alsea stock, the data were combined. For the
combined data, the AC (28% mortality) and CC
(24% mortality) genotypes were significantly
(P<O.OI) more resistant to BKD than was the AA
genotype (62% mortality). Within both the stocks
and transferrin genotypes, differences between
replicates were not significant.
The second BKD experiment with coho salmon
gave results similar to those of the first on the
basis of transferrin genotypes (Figure IB). Unfortunately, the AA genotype was not included in the
Alsea comparison because we lacked sufficient
fish. No stock comparison was made because the
Big Creek stock came directly from the hatchery,
at a time when 91.5% of the mortalities in production fish at Big Creek were due to BKD (J. Conrad5 ). The probability that the Big Creek coho
salmon used 'in the experiment had previously
been exposed to BKD was therefore very high.
In the third BKD study, which involved the four
steelhead stocks and a second Rogue stock reared
at the hatchery (Figure lC), mortalities in all the
test groups began to increase at a high rate 3 wk
after the study began because ofa secondary infection with Aeromonas hydrophila. This trend continued for another 4 wk, at which time mortalities
leveled off, and the study was terminated. A comparison of the resistance of the different stocks is
not fully valid because the fish in the different test
tanks were obviously not challenged equally with
a secondary infection of A. hydrophila. However,
there were no significant differences (P>O.IO) between replicates, and the mortality of the Siletz
steelhead trout (72%) was significantly lower
(P<0.05) than that of all other stocks except the
Alsea. Because mortality in the Rogue stock was
extremely high (96%), a transferrin genotype
comparison was not considered. The AC and CC
genotypes within the Alsea stock were equally
susceptible to the double infection of BKD and A.
hydrophila. Although percentage mortality is a
better measure ofan organism's ability to tolerate
disease, mean time to death is also an indication of
resistance to diseases, especially chronic ones such
as BKD. There were no differences in mean time to
death (days) among either the Rogue or Alsea
steelhead transferrin genotypes (numbers of fish
OJ. Conrad, Oregon Department of Fish and Wildlife,

Clatskanie, OR 97015, pers. commun. February 1978.

in parentheses): Rogue-AA, 28.5 (30); AC, 30.0

(41); and CC, 29.7 (19); Alsea-AC, 30.4 (21); and
CC, 30.0 (62). The importance of transferrin was
probably reduced by the double infection.

Vibriosis
In the first experiment in which coho salmon
.were exposed to V. anguillarum (Figure 2A), the
Big Creek stock (38 % mortality) was significantly
more resistant (P<0.005) than the Alsea stock
(62% mortality) (transferrin was not considered in
this comparison). There was a significant difference (P<0.005) in mean weight (t'-test, Snedecor
and Cochran 1967:114) between the Alsea and Big
Creek fish. However, there were no significant
differences (P>O.IO) in resistance to vibriosis
among four weight classes (5.1-10.0, 10.1-15.0,
15.1-20.0, and 20.1-25.0 g) within either stock.
The difference in resistance between the two
stocks appears to be genetic. In a second test, the
resistance trend between the Alsea and Big Creek
stocks was reversed (Figure 2B), though at a lower
level of significance (P<0.07) than the previous
experiment. However, the Alsea coho salmon used
in this second test came directly from the hatchery. Though it is unlikely that any of these fish
would have been previously exposed to V. anguillarum in freshwater, a difference in susceptibility
to vibriosis still existed. These conflicting results
thus demonstrate that the environment has a
strong effect in determining resistance to vibriosis. In both the Alsea and Big Creek stocks, no
differential resistance was shown by the transferrin genotypes, although the AA genotype was not
included in the Alsea transferrins (Figure 2B).
In the first ofthe two vibriosis experiments with
steelhead trout (Figure 2C), the North Santiam
steelhead trout were the least susceptible to vibriosis of all the stocks (P<0.05). The Alsea
steelhead trout, though exhibiting a higher mortality (87%) than the North Santiam fish, were
still significantly more resistant than the remaining two stocks (P<0.05). Because mortality was
high in the Smith Farm- and hatchery-reared
Rogue stocks (96%), transferrin genotype differences and the effects of rearing environment on
resistance were not considered. However, no differences in resistance were observed among
genotypes within the Alsea stock. These results
using steelhead trout are similar to those observed
in the coho salmon exposed to vibriosis.
The second vibriosis experiment (Figure 2D),
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FISHERY BULLETIN: VOL. 77, NO.4

VIBRIO-coho
100

100

VIBRIO-steel head

90

55

47

34 35

69

65

128

Cl

Cl

Cl

Cl

50

50

153

l-

I-

a:
w
a.

a:
w
a.

Z
w
U

STOCK

GENOTYPE

BIG CR.

ALSEA

STOCK

AC CC

VIBRIO-coho

SILETZ

43

9
11

T
N.SAN

VIBRIO-steelhead

100

100

ROGUE RQGUE(HI ALSEA

39 50
21

26

6B
34
17

51

Cl

14 14

FIGURE 2.-Percentages offish ofdifferent

stocks and transferrin genotypes that died
of vibriosis. A and B, coho salmon experiments 1 and 2; C and D, steelhead trout
experiments 1 and 2. For interpretation of
other features see Figure 1.

Cl

Cl

50

50

l-

I-

a:
w

a:
w
a.

Cl.

GENOTYPE AA AC T
STOCK

BIG CR.

AC CC

ALSEAIH)

GENOTYPE AA AC CC
STOCK

ROGUE (H)

AC CC T
ALSEA(H)

involving hatchery-reared steelhead trout from

the Rogue, Alsea, and North Santiam, revealed
the same results as did the first, with respect to
transferrin genotypes. No differential resistance
was shown among genotypes, including the AA's,
within either the Alsea or Rogue stocks. Although
resistance to vibriosis among the three stocks was
similar, the North Santiam stock showed the
highest mortalities this time-which again emphasizes the importance of environmental factors
in the determination of resistance and the need for
eliminating environmental differences in making
genetic comparisons. There was a significant dif-

800

T
N.SAN.{HI

ference in vertebral number between North Santiam steelhead trout reared at the hatchery and at
Smith Farm, indicating an environmental difference (our unpubl. data). The Rogue replicates in
this experiment were significantly different
(P<0.025) with respect to stock mortality; consequently a genetic comparison was invalid. Except for the hatchery-reared Rogue replicates in
the last vibriosis experiment usingsteelhead trout,
there were no significant differences between replicates for stocks or genotypes in all four vibriosis
tests; consequently we combined replicates in the
data analysis.

WINTER ET AL.: RESISTANCE OF COHO SALMON AND STEELHEAD TROUT

Perhaps stock resistance to acute diseases such

as vibriosis depends more on which stock has
an environmental advantage at the time of infection, rather than on genetic make-up. Also,
when mortalities in experiments are high, resistance comparisons are difficult to make because
any immunity that was present may have been
overwhelmed. Genetic factors are probably more
important in chronic diseases such as BKD. For
example, Zinn et al. (1977) observed apparent
genetic resistance to infection by Ceratomyxa
shasta, normally not an acute condition, among
hatchery strains of chinook salmon.
It is also evident that a stock may be resistant to
one disease and not to another. Although the
Siletz steelhead trout were most resistant to the
double infection of BKD and A. hydrophila, they
showed the greatest susceptibility to V. anguillarum. Ehlinger (1977) observed that certain
selected brook trout strains, though resistant to
furunculosis, were more susceptible to gill disease
than was the native stock. Consequently selection
of stocks for resistance to several diseases would
be difficult (McIntyre 1977), except possibly when
the pathogens are closely related (Hutt 1970).
Judging by the present results, it appears that
the importance of transferrin genotypes in resistance to disease is stock specific. Differences
among genotypes were only observed in the Alsea
and B x S coho salmon infected with BKD. Weinberg (1974) noted that different host species may
vary in the extent to which they rely on ironspecific nutritional immunity. Although only the
most common genotypes were compared within
each stock, it is unlikely that other genotypes
would have shown greater resistance to BKD;
their frequencies within the stocks would have
been increased by natural selection if the disease
plays an important role as a selective agent. However, it is apparent that factors other than disease
may select for different transferrin genotypes. In
Ukranian carp, Cyprinus carpio, general survival
rates were highest among individuals with the AC
genotype (Balakhnin and Galagan 1972). There is
also an association of transferrin phenotype with
weight gain in juvenile rainbow trout that may be
due to the linkage of the transferrin locus with a
gene or gene complex affecting growth (Reinitz
1977). The association of resistance to BKD with
transferrin genotype may also be due to a gene
linkage; if so, transferrin serves only as a marker.
McIntyre and Johnson (1977) observed higher
growth rates and better survival in AA than in AC

transferrin genotypes of Big Creek coho salmon.

While the frequency of the C allele is high in the
Alsea stock, that frequency is depressed in a mixed
population at Big Creek where Alsea coho salmon
have been used to supplement the broodstock (J.
D. McIntyre unpubl. data). Although BKD selects
for the C allele in the Alsea coho salmon, the
advantage of this allele is offset by some other
.more important selective factor, such as growth
rate, within the Big Creek stock.
It is also conceivable that transferrin genotypes
provide resistance to different diseases, or not at
all-as with vibriosis. The ability to synthesize
iron chelators-compounds necessary to remove
iron from transferrin-is considered a virulence
factor for certain pathogens (Arnold et al. 1977).
Perhaps the iron chelators of V. anguillarum remove iron from transferrin more efficiently than
do those of BKD bacteria. This more efficient removal would explain to some extent the lack of
differential resistance to vibriosis among
genotypes within both coho salmon and steelhead
trout stocks. Pratschner (1978) observed differential resistance among transferrin phenotypes to
vibriosis and several other diseases in coho salmon
from the Skagit River, Wash. The AA phenotype
exhibited greater susceptibility to vibriosis and
cytophagosis but greater resistance to furunculosis while the CC phenotype was most resistant
to vibriosis and very susceptible to furunculosis
and cytophagosis. The disparity between
Pratschner's and our results with respect to vibriosis may be due to the stock-specific nature of
transferrin. Possibly differences among transferrin genotypes are more significant in a chronic
disease such as BKD, and less so in an acute disease such as vibriosis-or perhaps the rapid death
rate following exposure to V. anguillarum compressed the results too much to allow differences to
be observed. Because of the short time span involved to vibriosis infections, the benefit of such
differences to individual fish would be negligible.
Keeping in mind such considerations as selection for transferrin genotypes by different factors
such as growth or disease, it becomes clear (as with
stocks) that selectively breeding for certain transferrin genotypes would not be advisable. Though
selection for one particular genotype might provide resistance to BKD, it might also entail lower
growth rates or even greater susceptibility to
other diseases. McIntyre (1977) cautiously recommended selective breeding for disease resistance only in propagated fish being held under
801

FISHERY BULLETIN: VOL. 77, NO.4

carefully controlled conditions or when one particular pathogen is a recurrent problem. Otherwise, it seems advisable to maintain variability in
a stock to meet the demands of a variable environment.

LITERATURE CITED
ARNOLD, R. R., M. F. COLE, AND J. R. MCGHEE.

1977. A bactericidal effect for human lactoferrin. Science (Wash., D.C.) 197:263-265.
BALAKHNIN, I. A., AND N. P. GALAGAN.
1972. Distribution and survival rate of individuals with
different transferrin types among carp offspring from various combinations of parents. Hydrobiol. J. 8(3):41-45.
EHLINGER, N. F.

1977. Selective breeding of trout for resistance to furunculosis. N.Y. Fish Game J. 24:25-36.
EVELYN, T. P. T.

1977. Immunization of salmonids. In Proceedings from

the International Symposium of Diseases of Cultured
Salmonids, April 4-6, 1977, p. 161-176. Tavolek, Inc.,
Seattle, Wash.
FRYER, J. L., J. S. NELSON, AND R. L. GARRISON.
1972. Vibriosis in fish. In R. W. Moore (editor), Progress
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